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Hypertonic saline-dextran suppresses burn-related cytokine secretion by cardiomyocytes

J W Horton1, D L Maass, J White

  • 1Department of Surgery, The University of Texas Southwestern Medical Center, Dallas, Texas 75390-9160, USA. JURETA.HORTON@utsouthwestern.edu

American Journal of Physiology. Heart and Circulatory Physiology
|March 15, 2001
PubMed

Insights

Hypertonic saline-dextran (HSD) improves heart function after burn trauma by reducing inflammatory cytokine release from cardiomyocytes. This treatment mitigates burn-induced cardiac dysfunction and inflammation.

Area of Science:

  • Cardiology
  • Trauma Research
  • Molecular Biology

Background:

  • Burn trauma impairs cardiac function.
  • Hypertonic saline-dextran (HSD) improves cardiac function post-burn.
  • The cardioprotective mechanisms of HSD are not fully understood.

Purpose of the Study:

  • To investigate if HSD alters cardiomyocyte tumor necrosis factor-alpha (TNF-alpha) secretion.
  • To determine the effect of HSD on cardiac contraction and relaxation after burn injury.
  • To elucidate the role of inflammatory cytokines in HSD-mediated cardioprotection.

Main Methods:

  • Wistar-Furth rats underwent burn injury and received either saline or HSD.
  • Hearts were isolated 24 hours post-burn for Langendorff perfusion or cardiomyocyte preparation.
  • Cardiomyocytes were stimulated with lipopolysaccharide (LPS) to measure cytokine secretion.

Main Results:

  • Burn trauma increased cardiomyocyte secretion of TNF-alpha, IL-1 beta, and IL-6, and worsened cardiac contraction.
  • HSD treatment in burn-injured rats reduced cardiomyocyte cytokine secretion and LPS-induced inflammatory response.
  • HSD treatment improved ventricular function in burn-injured rats.

Conclusions:

  • HSD downregulates cardiomyocyte inflammatory cytokine secretion after burn trauma.
  • Reduced cytokine secretion contributes to HSD-mediated cardioprotection.
  • HSD offers a potential therapeutic strategy for burn-induced cardiac dysfunction.

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